Chronic obstructive pulmonary disease (COPD) includes conditions such as, e.g., chronic bronchitis and emphysema. COPD currently affects over 15 million people in the United States alone and is currently the third leading cause of death in the country. The primary cause of COPD is the inhalation of cigarette smoke, responsible for over 90% of COPD cases. The economic and social burden of the disease is substantial and is increasing.
Chronic bronchitis is characterized by chronic cough with sputum production. Due to airway inflammation, mucus hypersecretion, airway hyperresponsiveness, and eventual fibrosis of the airway walls, significant airflow and gas exchange limitations result.
Emphysema is characterized by the destruction of the lung parenchyma. This destruction of the lung parenchyma leads to a loss of elastic recoil and tethering that maintains airway patency. Because bronchioles are not supported by cartilage like the larger airways, they have little intrinsic support and therefore are susceptible to collapse when destruction of tethering occurs, particularly during exhalation.
Inhaled cigarette smoke (and other noxious gases such as biomass smoke) cause lung inflammation, and this inflammatory response in COPD patients may lead to destruction of the lung parenchyma, emphysema, disruption of normal repair and defense mechanisms, and small airway fibrosis. Several pathological changes occur that can result in the narrowing of the airway lumen and the loss of the tethering function of the lung parenchyma, promoting a reduction of expiratory flow. These pathological changes include an inflammatory cell infiltrate, goblet-cell metaplasia, squamous-cell metaplasia, fibrosis, and an increased smooth-muscle mass.
One major symptom of COPD is reduced lung function, which is measured by Forced Expiratory Volume (FEV1). FEV1 defines the maximum volume of air that a person can forcibly breathe out in one second. FEV1 progressively decreases in COPD patients. COPD causes contraction, inflammation, and remodelling of the airways, increasing airflow resistance and lowering FEV1. Increased airflow resistance is particularly prevalent in the small airways (e.g., in airways having a diameter of 2 mm or less). Another complicating factor in COPD patients is excessive mucus secretion that can easily block an already small or narrow airway. In healthy individuals, there is no significant airflow limitation.
Hyperinflation is a clinical symptom of emphysema caused by air trapping whereby air can easily enter the parenchyma but becomes trapped by closing airways during exhalation. Emphysematic bula or voids can become permanently inflated causing remodelling of the chest, and a subsequent ‘barrel chested’ appearance. Also, during exercise, the inability to exhale rapidly causes dynamic hyperinflation that eases only by resting and by patients using a ‘pursed lip’ technique to deflate their lungs. This hyperinflation symptom causes extreme stress and anxiety to COPD patients.
Some bronchi and bronchioles may be partially or totally occluded by mucus plugs. The inflammatory changes in small airways may include acute inflammation and fibrosis. The changes in the diseased small airways are associated with two distinct components—one potentially reversible and the other irreversible. The potentially reversible component is related to mucus plugging, acute inflammation, and increased muscle tone due to hyper-responsivity. The irreversible component is related to fibrosis, distortion, narrowing due to tissue (e.g., muscle) thickening, and obliteration of small airways representing fixed obstruction in patients with COPD.
Many patients with COPD have a combination of small airways disease and emphysema. Studies have shown that the lower or dependent lung has a bigger impact on lung function and patients symptom than the upper lung. This is because emphysema is more severe in the upper lung, the relative size of each part of the lung, and the relative amount of respiration taking place in each part of the lung.
Collateral ventilation is the ability of gas to move from one part of the lung to another through nonanatomic pathways. The importance of collateral ventilation is minimal in normal, healthy lungs, because the resistance to air flow is higher in collateral channels than in the airways. However, the resistance of air flow in collateral channels is relatively low in patients with emphysema. In emphysematous lungs, collateral ventilation may provide important channels for gas distribution and may be therapeutically useful. In emphysema, the loss of tethering of the bronchioles in the lung parenchyma results in collapse on exhalation, which causes trapping of air and hyperinflation. The creation of direct passages between emphysematous pulmonary parenchyma and bronchial airways (airway bypass) may improve expiratory flow and volume and reduce hyperinflation.
In small airways disease, the narrowing and obliteration of the airways closes off access to distal healthy alveoli. However, these healthy alveoli do not undergo atelectasis, and thus, are likely being ventilated by collateral ventilation through the Pores of Kohn. Unfortunately, this ventilation is not adequate for respiration and CO2 can build up in the alveoli.
Thus, there remains a need for improved methods and devices that allow for better treatment of COPD patients. It may therefore be beneficial to provide techniques to treat the damaged lung system such that the more air can be transferred to and from the alveoli (for gas transfer) and increase FEV1.